mbH (Stuttgart) 76 (4) 627-31 (1996) tion of these patients was 78.7 seconds and was different from that of controls (p <0.004) (Table 2). Seven patients out of the nineteen had even lower values (<59.5 s). The mean APC-SR of these nineteen resistant patients was lower (mean ratio: 0.72, SD = 0.08) and signifi cantly different (mean ratio: 1.17, SD = 0.20; p <0.001) from that of controls. When APTT assays were evaluated to assess the ability of a defective plasma to correct the poor response to activated PC by mixing resistent plasma (1:1) with defective plasma, no cross-correlation between patients and controls was found (VC = 5.7%). Patients with the poor response to APC were reinvestigated in a range of time between 2 and 12 months from the first investigation. All had still a poor response to anticoagulant action of APC and the variation coeffi cient between the first and the second evaluation was always less than 6.5%. Genetic analyses evidenciated that among APC-resistant patients, 14 were heterozygous for FV Leiden mutation and 5, with the lowest APC-ratio values, were homozygous for the same missense mutation. The mean age of the nineteen resistant subjects was 28.5 years (range 22:42 y). By excluding a single patient who suffered from a TIA at 44 y, the mean age of the group was 27.3 years (r = 0.948, p <0.001). No subject with an APC resistance was found in the sixty controls. Sixty-eight percent (34/50) had plasma LDL cholesterol levels >1.35 g/1 and fourty-four percent (22/50) smoked more than 25 cigarettes/day. Eleven out of fifty patients (22%) had a positive family history for ischemic complications of atherosclerosis. Five of them had only one risk factor such as a positive family history or a defective APC-cascade. Thirty-two of the sixty relatives (53.3%) of the patients with the APC resistance showed a poor response to APC as well (mean APC ratio: 0.92, SD = 0.22). Eleven family members suffered from prior TIAs (19%). The frequency of APC-resistance in our patients appears to be at least 15-20 times as common as in the control subjects. Thus, our data are consistent with the possibility that we have selected young patients with familial defects in APC cascade. Stratified analysis for risk factors showed that 11 of 19 patients with APC-resistance reported a family history of TIAs, while no difference was observed in patients with or without high lipid plasma levels and hypertension. The relevance of these data with respect to potential new strategies of intervention in high risk-individuals, mostly in patients with familial risk, and the implications with respect to the data reported in an apparently healthy population of middle-aged individuals (6). suggest that appropriate model systems are needed to evaluate the relevance of abnormalities in the cerebrovascular thrombotic risk.
This study was done to test the clinical impression that the result of the oral glucose tolerance test could be used to predict which patients with gestational diabetes did not need insulin therapy. If this was true, a full blood sugar profile assessment could be avoided in many of these women. The second analysis was to test the clinical impression that the fasting glucose level was the best predictor of insulin requirement in women with gestational diabetes. The results of the study showed that none of the 3 readings of the oral glucose tolerance test could be used to predict reliably which patients did not need insulin therapy. Hence, blood sugar profile assessment of all patients with gestational diabetes is still necessary. The receiver-operator characteristic curves also showed that the 2-hour postload glucose level during the 75 g load glucose tolerance test was a better predictor of insulin requirement than the fasting glucose level.
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